Effects of
somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a
gastric fistula.
Intravenous infusion of small doses of
somatostatin (0.1-0.5 microgram/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of
somatostatin (0.5-2.5 micrograms/kg/min) also dose-dependently inhibited the
bethanechol-induced gastric acid secretion. The dose of
somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 microgram/kg/min for vagally stimulated
acid secretion and 2.5 micrograms/kg/min for
bethanechol-induced
acid secretion. Thus, the inhibitory potency of
somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on
bethanechol-induced
acid secretion.
Somatostatin had no effect on the increase in gastric MBF during
vagus nerve stimulation or
bethanechol infusion. Pretreatment with
indomethacin or
phentolamine had no effect on the inhibitory effect of
somatostatin on the increase in gastric acid secretion during
vagus nerve stimulation or
bethanechol infusion. These results suggest that
somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitory effect of
somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to
prostaglandin-involved or alpha
adrenoceptor-mediated mechanisms.